The anxiolytic effect of benzodiazepines is due to their binding to GABAA receptor at a site distinct from the GABA binding site (Whiting, 2003). To determine whether the anxiolytic-like effect of the EO in the LDB occurs through the GABAergic system, mice treated with the EO or DZP were co-administered FLU, a benzodiazepine GABAA site antagonist. This procedure reversed the anxiolytic-like activity of not only the standard drug DZP but also the EO (Fig. 2). The ability of FLU, a specific GABAA receptor antagonist, to antagonize the anxiolytic-like activity of the EO strongly suggests, for the first time, a role of this receptor complex in mediating EO activity. Furthermore, according to Silva et al. (2010) the EO from Cymbopogon citratus administered i.p. had anticonvulsant effect, by intraperitoneal route, which was blocked by the pretreatment with flumazenil, suggesting and enhancing a possible effect on the GABAergic neurotransmission system. The authors did not exclude a possible interference of other systems (e.g., glycinergic) in such activity.